High impact information on Cdc6

• Collectively, our data suggest that initiation of DNA replication is regulated by p53 through Cdc6 protein stability [1].
• p53-Dependent regulation of Cdc6 protein stability controls cellular proliferation [1].
• We show that activation of p53 by DNA damage results in enhanced Cdc6 destruction by the anaphase-promoting complex [1].
• Vitamin E supplementation resulted in higher expression of genes involved in cell cycle regulation (Ccnb2, Cdc2, Cdc6) in old T cells [2].
• Most factors including cyclins, Cdc6, and geminin are rather constitutively expressed during the cell cycle of ES cells [3].

Biological context of Cdc6

• Here we describe hamster cell lines with BAC transgenes that express mouse Cdc6 at levels that correlate with BAC copy number; show that mouse Cdc6 is regulated normally during the cell cycle, binds chromatin, and is degraded during apoptosis; and report a novel fraction of Cdc6 that associates with the spindle apparatus during mitosis [4].
• Functional analysis of bacterial artificial chromosomes in mammalian cells: mouse Cdc6 is associated with the mitotic spindle apparatus [4].
• An endothelin enhancer and Cdc6 promoter chimera drives expression of the IGF-IR ribozyme [5].
• As for the positive controls adozelesin and cisplatin, arrest was accompanied by phosphorylation of ATM kinase; dephosphorylation of pRB; decreases in RF-C, cyclin D1, Cdc25A, and Cdc6; and increases in p21 [6].
• The regulation of competence to replicate in meiosis by Cdc6 is conserved during evolution [7].

References